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2006 Progress Report: Research Project on Asthma: Prenatal and Postnatal Urban Pollutants and Childhood Asthma
EPA Grant Number: R832141C002Subproject: this is subproject number 002 , established and managed by the Center Director under grant R832141
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
Center: Columbia Center for Children’s Environmental Health
Center Director: Perera, Frederica P.
Title: Research Project on Asthma: Prenatal and Postnatal Urban Pollutants and Childhood Asthma
Investigators: Rothman, Paul B.
Institution: Columbia University
EPA Project Officer: Fields, Nigel
Project Period: November 1, 2003 through October 31, 2008
Project Period Covered by this Report: November 1, 2005 through October 31,2006
RFA: Centers for Children's Environmental Health and Disease Prevention Research (2003)
Research Category: Children's Health , Health Effects
Description:
Objective:The specific aims of the project are to: (1) determine the relationship between environmental exposures experienced prenatally through early childhood and atopy, adverse respiratory outcomes and asthma at age 5-7 years; (2) determine interaction between susceptibility factors and environmental exposures on respiratory outcomes and asthma through ages 5-7; (3) determine if (a) antigen-induced cord blood mononuclear cell (CBMC) proliferation or cytokine production increases the risk for decreased lung function or atopy at age 5 among children with probable asthma at age 2 years, (b) allergen-specific IgE levels at ages 2 and 3 years are associated with decreased lung function or atopy at age 5 years; and (4) collaborate with the Community Translation and Application Core (COTAC) to ensure that asthma risk factors of concern to the community are being addressed, translate research findings back to the community, and assist in developing interventions and policies to prevent exposures that contribute to asthma and adverse respiratory health in New York City and elsewhere.
Progress Summary:Recruitment of Study Participants
Recruitment of cohort is complete.
Data Collected
Questionnaire completion rates: 838 prior to delivery, 592 at 3 months, 588 at 6 months, 538 at 12 months, 432 at 24 months, 379 at 36 months, 279 at 60 months, and 143 at 72 months. Over 66 allergy skin tests, over 573 IgE analyses, and 213 lung function tests have been completed at age 5-6 years. Numbers will increase as children more recently enrolled into the study reach older ages. Airborne polycyclic aromatic hydrocarbon (PAH) data collected by the Exposure Core were used to analyze the relationship between prenatal exposure (airborne pyrene or PAHs and levels of mouse, cockroach, and dust mite allergens measured in home dust at child age 1 year) and the onset of allergic sensitization and respiratory symptoms through age 2 years.
Findings
Allergen-Specific IgE. There continues to be evidence of cockroach, mouse, and, more rarely, dust mite allergy as early as ages 2 and 3 years (Table 1). The frequency of sensitization to cockroach and dust mite is increasing between ages 2-5 years. A total of 16 percent of children had a positive allergen-specific IgE to at least one of the antigens at age 2 years. These frequencies were not affected by gender of the child, mother’s reported asthma, ethnicity, or mother’s IgE. Our results demonstrate that the allergic immune response to cockroach and mouse, allergens implicated in inner city asthma, can occur by age 2 years.
Table 1. Allergen-Specific IgE (% > 0.35 IU/ml)
|
|
Anti-Cockroach IgE |
Anti-Mouse |
Anti-Dermatophagoides farinae IgE |
|
Age 2 (n = 302) |
7.6 |
7.9 |
2.2 |
|
Age 3 (n = 202) |
8.9 |
6.5 |
3.5 |
|
Age 5 (n = 191) |
20.9 |
8.4 |
7.4 |
Frequency of Respiratory Symptoms. Respiratory symptoms and probable asthma were common (Figure 1). The presence of difficulty breathing and wheeze at age 2 years have been associated with an increased allergen-specific IgE at age 2 years (p = 0.004 and p = 0.023, respectively).
Figure 1. Frequency of Respiratory Symptoms
Prenatal PAH/Pyrene Exposure, ETS, and Allergic Immune Response
Increased levels of pyrene, but not allergen exposure, were associated modestly with anti-mouse IgE at age 2 years (r = 0.158, p = 0.012). Results suggest that early exposure to pyrene may upregulate allergic immune responses to mouse antigen by age 2. Among the initial 303 children prospectively followed through age 1 year, significantly more cough and wheeze were found among those who had both elevated prenatal PAH exposure and postnatal exposure to environmental tobacco smoke (ETS) (PAHxETS interaction OR = 1.41, p < 0.01 for cough; OR = 1.29, p < 0.05 for wheeze). By 2, difficulty breathing and probable asthma were reported more frequently in children exposed prenatally to elevated PAHs and ETS postnatally (PAHxETS OR = 1.54 difficulty breathing; OR = 1.64 probable asthma, both p < 0.05).
Prospective Association Between BMI at Age 3 Years and Specific IgE at Age 5 Years (n = 109)
Children with a body mass index (BMI) percentile for age at least at risk for being overweight were more likely to be making an IgE response to dust mite (RR 5.7 [1.3-25]) and cockroach (RR 1.6 [0.8-3.2]) at age 5 (Table 2). The association for cockroach was stronger (RR 2.3 [0.8-6.5]), when only children exposed (prenatal dust sample) to 0.75 μg/g Bla g 2 were analyzed. Similar, although less striking, trends were observed when BMI data from age 2 were examined. While most of these associations are not statistically significant, the sample size is quite small but growing. As demonstrated above, the period between 3-5 years represents an important age for the onset of allergen-specific IgE. The absence of an association between obesity and allergic sensitization in other studies may have been due to not evaluating the body fat and allergic sensitization early enough in life.
Table 2. Body Mass Index (BMI) at Age 3 and Allergen-Specific IgE at Age 5
|
|
BMI at Age 3 |
|
|
|
|
Normal |
At least at risk |
Risk Ratio |
|
Anti-Cockroach IgE |
18.0% |
29.2% |
1.6 [0.8-3.2] |
|
Anti-Mouse IgE |
11.5% |
6.3% |
0.54 [0.15-2.0] |
|
Anti-D. farinae |
3.3% |
18.8% |
5.7 [1.3-25] |
Pet Protective Effect
Both cat and dog ownerships were more common among the African-American (35% and 11%) than Dominican mothers (4% and 6%). Cat or dog ownership was inversely associated with allergic rhinitis symptoms at ages 1, 2, and 3 years (adjusted OR 0.68 [0.4-1.1], 0.46 [0.3-0.8], and 0.48 [0.2-0.9], respectively). There were no associations between cat or dog ownership and wheeze at any of these ages (0.91 [0.6-1.5], 1.1 [0.7-2.1], and 0.95 [0.4-2.0], respectively). Among cat/dog owners, specific IgE at 5 years was less common to cockroach (9.7% vs. 24%, p = 0.09) and D. farinae (0% vs.12%, p = 0.038) with no difference for IgE to mouse (9.7% vs.10%). No association was observed with dog ownership.
Significance
The full significance of our results with respect to asthma causation is not known given the young age of the cohort. Our results support an important early role of the environment in asthma pathogenesis. Specifically: (1) early exposure to airborne PAHs and ETS can lead to increased respiratory symptoms and probable asthma by age 1 to 2 years; (2) elevated total and allergen-specific IgE levels, and possibly early signs of asthma, occur at an early age; (3) obesity may predispose to not only asthma (data not shown), but allergy; and (4) early exposure to pets may protect against atopy, but not wheeze.
Future Activities:We plan to continue expanding data collection and analysis. Evaluation of the relationship between birth biomarkers and findings at age 2 through 7 years is ongoing. Evaluation of modifying effects of obesity and the pet protective effect are underway.
Journal Articles:No journal articles submitted with this report: View all 2 publications for this subproject
Supplemental Keywords:children’s health, health effects, health risk assessment, asthma, genetics, assessment of exposure, PAH, ETS, environmental risks, environmental exposure, exposure assessment, genetic risk factors, genetic susceptibility, maternal exposure, nutritional risk factors,
, HUMAN HEALTH, ENVIRONMENTAL MANAGEMENT, Scientific Discipline, Health, RFA, Health Effects, Risk Assessment, Health Risk Assessment, Epidemiology, Children's Health, Biochemistry, Genetics, exposure assessment, genetic risk factors, children's environmental health, diesel exhaust, assessment of exposure, prenatal exposure, genetic susceptibility, maternal exposure, nutritional risk factors, genetic mechanisms, environmental risks, asthmaRelevant Websites:
http://www.mailman.hs.columbia.edu/ccceh/ 
Progress and Final Reports:
2004 Progress Report
2005 Progress Report
Original Abstract
Main Center Abstract and Reports:
R832141 Columbia Center for Children’s Environmental Health
Subprojects under this Center:
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
R832141C001 Growth and Development Research Project: Prenatal and Postnatal Urban Pollutants and Neurobehavioral Developmental Outcomes
R832141C002 Research Project on Asthma: Prenatal and Postnatal Urban Pollutants and Childhood Asthma
R832141C003 Mechanistic Research Project
R832141C004 Community-Based Intervention Project: Reduction of Exposure and Risk from Pesticides and Allergens
R832141C005 Community Translation and Application Core (COTAC)
R832141C006 Exposure Assessment Facility Core
R832141C007 Data Management, Statistics and Community Impact Modeling Core
R832141C008 Administrative Core